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The involvement of thromboxane A2 (TXA2) in systemic inflammation and infection is well recognized. However, there are few reports on the involvement of prostanoids in warm shock (the initial pathology of sepsis). Previous studies showed that interleukin (IL)-1β causes a rapid inducible nitric oxide synthase/nitric oxide (iNOS/NO)-mediated relaxation in peripheral blood vessels during warm shock. Furthermore, a transient contraction was seen before this relaxation occurred. The present study aimed to elucidate the mechanism of this transient contraction. We measured isometric tension changes in the superior mesenteric arteries from normal male Wistar rats by adding IL-1β at the point of maximum contraction by phenylephrine (Ph). The same study was performed for each vessel pretreated with various inhibitors, including SQ29548, a TXA2 receptor antagonist, 30 min before Ph contraction. In addition, the concentration of thromboxane B2 (TXB2) in SMA was measured by probe electrospray ionization. Treatment of endothelial vessels with cyclooxygenase 1 (COX1)/2 inhibitors SC560/NS398 and TXA2 receptor antagonist SQ29548 suppressed IL-1β–induced transient contractions. This transient contraction reaction was derived from TXA2. Additionally, gene expression of COX2/TXA2 synthetase and the concentration of TXB2 were significantly increased in IL-1β-exposed vessels. It was demonstrated for the first time in inflamed blood vessels that endothelial cell-derived COX2/TXA2 is induced before iNOS and causes transient contractions. TXA2 may be considered an early sign of warm shock or as a biological defense mechanism in the early stages of septic shock.

Arterial thromboxane A2-induced transient contraction after IL-1β exposure